Rosemarinic Acid-Induced Destabilization of Aβ Peptides: Insights from Molecular Dynamics Simulations.

Alzheimer's disease (AD) is a neurodegenerative disorder marked by the progressive accumulation of amyloid-β (Aβ) plaques and tau protein tangles in the brain. These pathological aggregates interfere with neuronal function, leading to the disruption of cognitive processes, particularly memory. The deposition of Aβ forms senile plaques, while tau protein, in its hyperphosphorylated state, forms neurofibrillary tangles, both of which contribute to the underlying neurodegeneration observed in AD.

An evaluation model for interactive gaming furniture design based on parent-child behavior.

This study takes the parent-child game behavior of children aged 3~6 and their parents as the research object, and extracts and summarizes the user behavioral needs of parents and children when they use game-based furniture together by using the questionnaire research method, observation method, and interview method. Based on the KJ method, 16 behavioral demand indicators were compiled by five furniture design students to construct a user behavioral demand system. In addition, AHP and entropy weight method were used to solve the user behavioral demand weights from subjective and objective perspectives in this study.

Tumor-targeted metabolic inhibitor prodrug labelled with cyanine dyes enhances immunoprevention of lung cancer.

Recent progress in targeted metabolic therapy of cancer has been limited by the considerable toxicity associated with such drugs. To address this challenge, we developed a smart theranostic prodrug system that combines a fluorophore and an anticancer drug, specifically 6-diazo-5-oxo-l-norleucine (DON), using a thioketal linkage (TK). This system enables imaging, chemotherapy, photodynamic therapy, and on-demand drug release upon radiation exposure.

and as a Prognostic Biomarker Correlated with Immune Infiltrates in Colorectal Cancer: Evidence from Bioinformatic Analysis.

The extensive morbidity of colorectal cancer (CRC) and the inferior prognosis of terminal CRC urgently call for reliable prognostic biomarkers. For this, we identified 704 differentially expressed genes (DEGs) by intersecting three datasets, GSE41328, GSE37364, and GSE15960 from Gene Expression Omnibus database, to maximize the accuracy of the results. Preliminary analysis of the DEGs was then performed using online gene analysis datasets, such as DAVID, UCSC Cancer Genome Browser, CBioPortal, STRING, and UCSC Cancer Genome Browser.

A critical update on the strategies towards small molecule inhibitors targeting Serine/arginine-rich (SR) proteins and Serine/arginine-rich proteins related kinases in alternative splicing.

>90% of genes in the human body undergo alternative splicing (AS) after transcription, which enriches protein species and regulates protein levels. However, there is growing evidence that various genetic isoforms resulting from dysregulated alternative splicing are prevalent in various types of cancers. Dysregulated alternative splicing leads to cancer generation and maintenance of cancer properties such as proliferation differentiation, apoptosis inhibition, invasion metastasis, and angiogenesis.

Mitochondrial TXNRD3 confers drug resistance via redox-mediated mechanism and is a potential therapeutic target in vivo.

Alterations in ROS metabolism and redox signaling are often observed in cancer cells and play a significant role in tumor development and drug resistance. However, the mechanisms by which redox alterations impact cellular sensitivity to anticancer drugs remain elusive. Here we have identified the mitochondrial isoform of thioredoxin reductase 3 (mtTXNRD3), through RT-PCR microarray screen, as a key molecule that confers drug resistance to sorafenib and other clinical anticancer agents.

Metabolic reprogramming and redox adaptation in sorafenib-resistant leukemia cells: detected by untargeted metabolomics and stable isotope tracing analysis.

Background: Internal tandem duplications (ITD) within the juxtamembrane domain of FMS-like tyrosine kinase 3 (FLT3) represent a poor prognostic indicator in acute myeloid leukemia (AML). Therapeutic benefits of tyrosine kinase inhibitors, such as sorafenib, are limited due to the emergence of drug resistance. While investigations have been conducted to improve the understanding of the molecular mechanisms underlying the resistance to this FLT3 inhibitor, a profile of cell functioning at the metabolite level and crosstalk between metabolic pathways has yet to be created.

Identification of cisplatin sensitizers through high-throughput combinatorial screening.

cis-Diamminedichloroplatinum/cisplatin (CDDP) is a major drug used in cancer chemotherapy; however, the toxic side-effects and development of drug resistance represent major challenges to the clinical use of CDDP. The aim of the present study was to identify effective drug combination regimens through high-throughput drug screening that can enhance the efficacy of CDDP, and to investigate the underlying mechanisms. A cell-based high-throughput screening methodology was implemented, using a library of 1,280 Food and Drug Administration (FDA)-approved drugs, to identify clinical compounds that act synergistically with CDDP.

B cell lymphoma with different metabolic characteristics show distinct sensitivities to metabolic inhibitors.

Cancer cells exhibit profound alterations in their metabolism (abnormal glucose and glutamine metabolism). Targeting cancer metabolism is a promising therapeutic strategy. Lymphoma can be classified into many different types and it is very complicated.